indication

For treatment of osteoarthritis and rheumatoid arthritis.

pharmacology

Piroxicam is in a class of drugs called nonsteroidal anti-inflammatory drugs (NSAIDs). Piroxicam works by reducing hormones that cause inflammation and pain in the body. Piroxicam is used to reduce the pain, inflammation, and stiffness caused by rheumatoid arthritis and osteoarthritis.

mechanism of action

The antiinflammatory effect of Piroxicam may result from the reversible inhibition of cyclooxygenase, causing the peripheral inhibition of prostaglandin synthesis. The prostaglandins are produced by an enzyme called Cox-1. Piroxicam blocks the Cox-1 enzyme, resulting into the disruption of production of prostaglandins. Piroxicam also inhibits the migration of leukocytes into sites of inflammation and prevents the formation of thromboxane A2, an aggregating agent, by the platelets.

toxicity

Symptoms of overdose include drowsiness, nausea, stomach pain, and/or vomiting.

biotransformation

Renal

absorption

Well absorbed following oral administration.

half life

30 to 86 hours

route of elimination

Piroxicam and its biotransformation products are excreted in urine and feces, with about twice as much appearing in the urine as in the feces. Approximately 5% of a piroxicam dose is excreted unchanged. However, a substantial portion of piroxicam elimination occurs by hepatic metabolism. Piroxicam is excreted into human milk.

drug interactions

Acebutolol: Risk of inhibition of renal prostaglandins

Acenocoumarol: The NSAID, piroxicam, may increase the anticoagulant effect of acenocoumarol.

Alendronate: Increased risk of gastric toxicity

Anisindione: The NSAID, piroxicam, may increase the anticoagulant effect of anisindione.

Atenolol: Risk of inhibition of renal prostaglandins

Betaxolol: Nonsteroidal Anti-Inflammatory Agents such as piroxicam may diminish the antihypertensive effect of Beta-Blockers such as betaxolol. Monitor for increases in blood pressure if a nonsteroidal anti-inflammatory agent (NSAID) is initiated/dose increased, or decreases in blood pressure if a NSAID is discontinued/dose decreased; this is particularly important if NSAID treatment is for extended periods of time. Ophthalmic beta-blockers are likely of little concern.

Bevantolol: Risk of inhibition of renal prostaglandins

Bisoprolol: Risk of inhibition of renal prostaglandins

Carteolol: Risk of inhibition of renal prostaglandins

Carvedilol: Risk of inhibition of renal prostaglandins

Colesevelam: Bile acid sequestrants may decrease the absorption of Nonsteroidal Anti-Inflammatory Agents. Monitor for decreased serum concentrations/therapeutic effects of nonsteroidal anti-inflammatory agents (NSAID) if coadministered with bile acid sequestrants. Separating the administration of doses by 2 or more hours may reduce (but not eliminate) the risk of interaction. The manufacturer of colesevelam recommends that drugs should be administered at least 1 hour before or 4 hours after colesevelam.

Cyclosporine: Monitor for nephrotoxicity

Dicumarol: The NSAID, piroxicam, may increase the anticoagulant effect of dicumarol.

Esmolol: Risk of inhibition of renal prostaglandins

Ginkgo biloba: Additive anticoagulant/antiplatelet effects may increase bleed risk. Concomitant therapy should be avoided.

Labetalol: Risk of inhibition of renal prostaglandins

Lithium: The NSAID, piroxicam, may decrease the renal excretion of lithium. Increased risk of lithium toxicity.

Methotrexate: The NSAID, piroxicam, may decrease the renal excretion of methotrexate. Increased risk of methotrexate toxicity.

Metoprolol: Risk of inhibition of renal prostaglandins

Nadolol: Risk of inhibition of renal prostaglandins

Oxprenolol: Risk of inhibition of renal prostaglandins

Penbutolol: Risk of inhibition of renal prostaglandins

Pindolol: Risk of inhibition of renal prostaglandins

Practolol: Risk of inhibition of renal prostaglandins

Propranolol: Risk of inhibition of renal prostaglandins

Ritonavir: Ritonavir increases the toxicity of piroxicam

Sotalol: Risk of inhibition of renal prostaglandins

Tamoxifen: Piroxicam may reduce clearance rate of Tamoxifen. Monitor for changes in therapeutic/adverse effects of Tamoxifen if Piroxicam is initiated, discontinued or dose changed.

Telmisartan: Concomitant use of Telmisartan and Piroxicam may increase the risk of acute renal failure and hyperkalemia. Monitor renal function at the beginning and during treatment.

Timolol: Risk of inhibition of renal prostaglandins

Tolbutamide: Piroxicam, a strong CYP2C9 inhibitor, may decrease the metabolism and clearance of Tolbutamide, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in Tolbutamide therapeutic and adverse effects if Piroxicam is initiated, discontinued or dose changed.

Torasemide: Piroxicam, a strong CYP2C9 inhibitor, may increase the serum concentration of Torasemide, a CYP2C9 substrate, by decreasing Torasemide metabolism and clearance. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of Torasemide if Piroxicam is initiated, discontinued or dose changed.

Trandolapril: The NSAID, Piroxicam, may reduce the antihypertensive effect of Trandolapril. Consider alternate therapy or monitor for changes in Trandolapril efficacy if Piroxicam is initiated, discontinued or dose changed.

Treprostinil: The prostacyclin analogue, Treprostinil, may increase the risk of bleeding when combined with the NSAID, Piroxicam. Monitor for increased bleeding during concomitant thearpy.

Triflusal: The metabolite of triflusal, 2-hydroxy-4-trifluoro-methyl-benzoic acid (HTB), impairs the serum protein binding of glisentide to the same extent as acetylsalisylic acid. Thus, the free fraction of glisentide may be increased. A dosage reduction may be required if used in combination.

Trimethoprim: The strong CYP2C9 inhibitor, Piroxicam, may decrease the metabolism and clearance of Trimethoprim, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimethoprim if Piroxicam is initiated, discontinued or dose changed.

Vilazodone: Increased risk of bleeding with concomitant use of NSAIDs and vilazodone

Voriconazole: Piroxicam, a strong CYP2C9 inhibitor, may increase the serum concentration of voriconazole by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of voriconazole if piroxicam is initiated, discontinued or dose changed.

Warfarin: Piroxicam, a strong CYP2C9 inhibitor, may decrease the metabolism of warfarin. The antiplatelet effect of piroxicam may also increase the bleed risk associated with warfarin. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of warfarin if piroxicam is initiated, discontinued or dose changed.